Author: Jefferson H. Dickey MD

Health Effects: American Thoracic Society (ATS) Summary

ATS Summary / Introduction

The summary of pre-1996 data above essentially reflects the thinking in the medical literature prior to 1996, which is about when most of the major academic reviews were published in anticipation of the EPA revision of the NAAQS for ozone and particulate. The pre-1996 data is perhaps best summarized by the review published by the Committee of the Environmental and Occupational Health Assembly of the American Thoracic Society in January 1996.3 This provides a convenient and expert point of departure for a review of the more recent research. I have excerpted the relevant conclusions from this 50 page review tome.

ATS Summary / Ozone

"Ambient air O3 is generated in the troposphere from precursors (hydrocarbons and NOx) in complex reactions catalyzed by light energy. ... During acute O3 exposure, many children and young adults progressively develop substernal pain on deep inspiration, irritative cough, and a reduced vital capacity and FEV1. These changes recede initially fairly rapidly and then somewhat more slowly over a period of several hours after exposure cessation, though some FEV1 decrement and symptoms may persist for as long as 24 hours.

"There is evidence from animal and human studies that certain alveolar macrophage antimicrobial defense functions are impaired after exposure to O3. In mice, O3-impaired macrophage function contributes to increased mortality after challenge with aerosolized inhaled bacteria, although in humans O3 exposure has not been shown to be directly associated with increased morbidity from respiratory infections.

"Acute exposure to O3 also provokes an upper and lower airway inflammatory response that includes mucosal hyperemia, increased permeability to serum proteins and to water soluble probe molecules placed on the airway surface, and infiltration of the mucosa with neutrophils. O3 exopsure also results in a large increase in inflammatory mediators and factors present in bronchial and alveolar lining fluids. Many of these mediators are likely released by epithelial cells in the lung. In view of the potent irritant like effects of O3 on the airways and of O3 induced bronchial hyperreactivity and airway inflammation, one might expect individuals with chronic airways disease to exhibit enhanced acute susceptibility to this pollutant. Indeed, studies of panels of asthmatics in the Los Angeles and Houston areas relating symptoms and medication use to air pollution levels, and associations between fluctuations in summertime O3 levels and hospital admissions from asthma, lend some support to this hypothesis. However, the reality is that O3 and other pollutants such as sulfates and acid aerosols commonly rise together, and, for this reason, it is difficult to attribute increased acute respiratory admissions to a single pollutant.

"Long term exposures of animals to O3 do not result in diffuse parenchymal lesions such as emphysema or diffuse fibrosis nor are pressure-volume curves usually displaced. However, there appears to be an emerging consensus that the principal effect of chronic O3 exposure in animals is a centri-acinar lesion in the terminal or respiratory bronchioles in which metaplastic airways epithelium extends into the proximal acinar regions accompanied by peribronchiolar mononuclear infiltrates, localized deposition of collagen, and remodeled peribronchiolar airspace. More severe degrees of injury are accompanied by restrictive impairments in airflow. These findings indicate the importance of and support the need for additional longitudinal and cross sectional population studies to look for evidence of excessive obstructive airways impairment among residents of perennially O3 polluted areas in the Los Angeles basin or elsewhere."

ATS Summary / Particulates

"Particles, SOx, and acid aerosols are a complex group of distinct pollutants that have common sources and usually covary in concentration. During the past two decades, the chemical characteristics and the geographic distribution of sulfur oxide and particulate pollution have been altered by control strategies, specifically taller stacks for power plants, put in place in response to air pollution regulations adopted in the early 1970s. While the increasing stack heights have lowered local ambient levels, the residence time of SOx and particles in the air have been increased, thereby promoting transformation to various particulate sulfate compounds, including acidic sulfates. These sulfate particles constitute a large fraction of the total mass of smaller particles (< 3 microns in aerodynamic diameter). Epidemiologic studies have consistently provided evidence of adverse health effects of these air pollutants. Particulate and SO2 pollution were strongly implicated in the acute morbidity and mortality associated with the severe pollution episodes in Donora (Pennsylvania), London, and New York in the 1940s, 1950s, and 1960s. There is new evidence that even current ambient levels of PM10 (30 to 150 micrograms/m3) are associated with increases in daily cardiorespiratory mortality and in total mortality, excluding accidental and suicide deaths. These associations have been shown in many different communities, as widely different in particle composition and climate as Philadelphia, St. Louis, Utah Valley, and Santa Clara County, California. It has recently been shown in a long-term prospective study of adults in the United States that chronic levels of higher PM10 pollution are associated with increased mortality after adjusting for several individual risk factors. Daily fluctuations in PM10 levels have also been shown to be related to acute respiratory hospital admissions in children, to school and kindergarten absences, to decrements in peak flow rates in normal children, and to increased medication use in children and adults with asthma. Although some epidemiologic studies suggest that acid aerosols are an important toxic component of PM10, other studies do not support this hypothesis. Dockery and Pope (408) recently reviewed the epidemiologic literature for adverse effects, assuming that reported associations can be attributed to acute particle mass exposures. Combined effects were estimated as percent increase in comparable measures of mortality and morbidity, associated with each 10 micrograms/m3 increase in daily mean PM10 exposure (Table 7). While total mortality increased by 1% for each 10 micrograms/m3 increase in PM10, respiratory mortality increased by 3.4% and cardiovascular mortality increased by 1.4%. Hospital admissions and emergency department visits increased approximately 1% for all respiratory complaints, and 2% to 3% for asthma. Exacerbation of asthma increased by about 3%, as did lower respiratory symptoms. Small decreases in lung function, approximately 0.1%, have also been observed. This review suggests that the epidemiologic studies of adverse morbidity measures are coherent with the mortality studies showing quantitatively similar adverse effects of acute exposures to particulate pollution."